The eyes of 20 normal mature Swiss albino rats were fixed by intracameral perfusion with glutaraldehyde at various levels of intraocular pressure (10, 20, 30 and 40 mmHg). The anterior chamber was connected by a fine cannula to a reservoir of fixative for 10 minutes while the animal was maintained under anaesthesia for a further 20 minutes after death. Five animals were studied at each pressure. Fixation at 0 mmHg was achieved by rapid immersion of enucleated eyes from 5 animals whose eyes had been cannulated and open to atmospheric pressure for the first 10 minutes. The anterior segment tissues were studied by light microscopy and by scanning and transmission electron microscopy. The eyes from rats fixed by cardiac perfusion provided control tissue. Progressive increase in intraocular pressure produced varying degrees of structural alterations in the iridocroneal angle. These included widening of the ciliary cleft and enlargement of the spaces of Fontana; however, the pectinate ligaments remained intact even at the highest pressure. The trabecular tissues became more distended and there was a statistically significant relationship between the fixation pressure and the mean number of giant vacuoles in the inner wall of Schlemm's canal. The response between animals fixed at the same pressure was variable. This was most pronounced at 10 and 40 mmHg. The results indicate that the rat outflow system responds morphologically to various levels of experimentally induced intraocular pressure in a similar fashion to primates. These findings, together with the morphological similarities between the rat and primate aqueous humour outflow pathways, particularly the presence of a single canal of Schlemm, suggest that the rat may be a valuable model for future studies of the normal and abnormal mechanisms of aqueous drainage. The technical difficulties of experimental studies of the aqueous drainage mechanism in such a small eye are discussed.
|Number of pages||16|
|Journal||Journal of Anatomy|
|Publication status||Published - 1 Jan 1989|